Unknown,Transcriptomics,Genomics,Proteomics

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Activating c-KIT mutations confers oncogenic cooperativity and rescue RUNX1-ETO induced DNA-damage in human cells

ABSTRACT: REtr causes genomic instability in U937 cells. Activated forms of c-KIT, like c-KIT(N822K), rescues the Retr induced genomic instability by increasing the rate of DNA repair by homologous recombination Human U937 cells were transduced with retroviral vectors encoding REtr or c-KIT(N822K), expanded in culture and FACS selected prior to molecular analysis

ORGANISM(S): Homo sapiens

SUBMITTER: Claudia Doring 

PROVIDER: E-GEOD-57658 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors.

Wichmann C C   Quagliano-Lo Coco I I   Yildiz Ö Ö   Chen-Wichmann L L   Weber H H   Syzonenko T T   Döring C C   Brendel C C   Ponnusamy K K   Kinner A A   Brandts C C   Henschler R R   Grez M M  

Leukemia 20140604 2

The RUNX1/ETO (RE) fusion protein, which originates from the t(8;21) chromosomal rearrangement, is one of the most frequent translocation products found in de novo acute myeloid leukemia (AML). In RE leukemias, activated forms of the c-KIT tyrosine kinase receptor are frequently found, thereby suggesting oncogenic cooperativity between these oncoproteins in the development and maintenance of t(8;21) malignancies. In this report, we show that activated c-KIT cooperates with a C-terminal truncated  ...[more]

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